Abstract

Cardiac troponin testing is front and center for the diagnosis of acute myocardial infarction (MI) in patients with signs and symptoms suggestive of an acute coronary syndrome, and in the absence of an ST-segment elevation on their electrocardiogram. For at least 15 years, the troponin concentration on presentation or the peak value during hospitalization has been recognized to carry both short- and long-term prognostic information. More recently, longitudinal follow-up of biomarkers after an MI has led to the recognition that patients with persistent increases in cardiac troponin or natriuretic peptide concentrations also have a poor prognosis compared with post-MI patients who have a decrease in concentrations (1, 2). With the recent evolution to “high-sensitivity” cardiac troponin assays, which can achieve a 10-fold increase in low-end sensitivity compared with their contemporary counterparts, detectable troponin concentrations can now be measured in 25%–67% of the general population, depending on the patient's age (3, 4). Even these low-level increases are not benign in these seemingly asymptomatic individuals, because such increases are associated with an increased risk of adverse cardiovascular events, including MI. Although cardiac imaging can provide some insight into the cardiac pathology underlying a persistent biomarker increase after an MI or in the general population, imaging still provides limited insight into a longitudinal process, given the cross-sectional nature of an imaging study. For example, in a patient with a high coronary calcium score according to computed tomography and an increased left ventricular mass by echocardiography, it is difficult to determine whether a detectable cardiac troponin concentration is due to a clinically unrecognized MI or to a persistent increase caused by myocardial pathology. Examples of 2 possible post-MI patterns for patients identified with a chronic troponin increase are shown in Fig. 1. Over an extended period of time, the patient with …

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